Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.7
3.4
Journals
Metabolites
Special Issues
Developmental Programming of the Hypothalamus and Metabolic Systems
share announcement

Developmental Programming of the Hypothalamus and Metabolic Systems

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 8693

Special Issue Editors

Prof. Sebastien G. Bouret

E-Mail Website
Guest Editor
Inserm, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Lille Neuroscience & Cognition Research Center, UMR-S 1172, 59000 Lille, France
Interests: neuroendocrinology; hypothalamus; development; obesity; nutrition
Dr. Sophie Croizier

E-Mail Website
Guest Editor
Center for Integrative Genomics, University of Lausanne, Genopode Building, 1015 Lausanne, Switzerland
Interests: hypothalamus; wiring; energy and glucose metabolism

Special Issue Information

Dear Colleagues,

The growing prevalence of metabolic and neuropsychiatric diseases is a major health concern, including among children. Epidemiological and animal studies suggest that alterations to the perinatal environment during critical periods of development, such as fetal and early postnatal life, are associated with increased risk of obesity, hypertension, and type 2 diabetes in later life. There is general recognition that the developing fetus and neonate is highly susceptible to adverse conditions such as maternal obesity and/or malnutrition, as well as perinatal stress. In particular, there is growing evidence that the developmental programming of metabolic systems, including the brain, pancreas, liver, heart, and adipose tissue, by the perinatal environment contributes to the global increase in obesity and metabolic diseases observed in modern society. The placenta, which plays a critical role in communication between mother and fetus, is also sensitive to changes in the nutritional environment and thus also contributes to the programming of metabolic disease. This Special Issue of Metabolites, “Developmental Programming of the Hypothalamus and Metabolic Systems”, will include original papers and review articles on the cellular, molecular, and behavioral mechanisms underlying the actions of perinatal factors (including metabolic and stress hormones, nutrition, pollutants, etc.) in the development and organization of metabolic systems that regulate body weight, energy balance, glucose homeostasis, and the stress axis.

Prof. Sebastien G. Bouret
Dr. Sophie Croizier
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hypothalamus
  • neuroendocrinology
  • perinatal nutrition
  • perinatal stress
  • metabolic programming
  • obesity
  • diabetes
  • developmental origins of health and adult disease

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

15 pages, 3126 KiB  
Article
Mouse Microglial Calcitonin Receptor Knockout Impairs Hypothalamic Amylin Neuronal pSTAT3 Signaling but Lacks Major Metabolic Consequences
by Bernd Coester, Thomas A. Lutz and Christelle Le Foll
Metabolites 2022, 12(1), 51; https://doi.org/10.3390/metabo12010051 - 8 Jan 2022
Cited by 3 | Viewed by 2530
Abstract
Amylin and leptin synergistically interact in the arcuate nucleus of the hypothalamus (ARC) to control energy homeostasis. Our previous rodent studies suggested that amylin-induced interleukin-6 release from hypothalamic microglia may modulate leptin signaling in agouti-related peptide expressing neurons. To confirm the physiological relevance [...] Read more.
Amylin and leptin synergistically interact in the arcuate nucleus of the hypothalamus (ARC) to control energy homeostasis. Our previous rodent studies suggested that amylin-induced interleukin-6 release from hypothalamic microglia may modulate leptin signaling in agouti-related peptide expressing neurons. To confirm the physiological relevance of this finding, the calcitonin receptor (CTR) subunit of the amylin receptor was selectively depleted in microglia by crossing tamoxifen (Tx) inducible Cx3cr1-CreERT2 mice with CTR-floxed mice. Unexpectedly, male mice with CTR-depleted microglia (KO) gained the least amount of weight of all groups regardless of diet. However, after correcting for the tamoxifen effect, there was no significant difference for body weight, fat mass or lean mass between genotypes. No alteration in glucose tolerance or insulin release was detected. However, male KO mice had a reduced respiratory quotient suggesting a preference for fat as a fuel when fed a high fat diet. Importantly, amylin-induced pSTAT3 was decreased in the ARC of KO mice but this was not reflected in a reduced anorectic response. On the other hand, KO mice seemed to be less responsive to leptin’s anorectic effect while displaying similar ARC pSTAT3 as Tx-control mice. Together, these data suggest that microglial amylin signaling is not a major player in the control of energy homeostasis in mice. Full article
(This article belongs to the Special Issue Developmental Programming of the Hypothalamus and Metabolic Systems)
►▼ Show Figures

Graphical abstract

10 pages, 739 KiB  
Article
Predicting Hair Cortisol and Cortisone Concentration in Postpartum Women through Repeated Measurements of Perceived Stress
by Jessica Lang, Susanne Stickel, Petra M. Gaum, Ute Habel, Jens Bertram, Simon B. Eickhoff and Natalia Chechko
Metabolites 2021, 11(12), 815; https://doi.org/10.3390/metabo11120815 - 29 Nov 2021
Cited by 13 | Viewed by 2614
Abstract
To investigate whether hair cortisol (HCC) and hair cortisone (HCNC) can be predicted by repeated stress reports from postpartum women in different mental health conditions (non-depressed, ND, adjustment disorder, AD, postpartum depression, PPD), 240 mothers (mean age 31.8 years; SD = 4.7) were [...] Read more.
To investigate whether hair cortisol (HCC) and hair cortisone (HCNC) can be predicted by repeated stress reports from postpartum women in different mental health conditions (non-depressed, ND, adjustment disorder, AD, postpartum depression, PPD), 240 mothers (mean age 31.8 years; SD = 4.7) were monitored from within 1 to 6 days of childbirth over a period of three months. HCC and HCNC in 3 cm hair samples were assessed via triple mass spectrometry after liquid chromatographic separation. Every second day, participants reported their stress levels online. The summed perceived stress scores were not found to be predictive of HCC. However, perceived stress predicted a decrease in HCNC (rSpearman = –0.153, p = 0.035) and an increase in the HCC/HCNC ratio (rSpearman = 0.304, p < 0.001) in the ND group. With AD in the first few weeks after childbirth, an inverse effect appeared for HCNC (rSpearman = 0.318, p = 0.011), suggesting an overall downregulation of the HPA axis owing to the stressful experience of adjusting to the new situation. No effects were found for mothers developing PPD. The indirect results of HPA-axis activity are better indicators of the experience of psychological stress in postpartum women than the absolute HCC value. Full article
(This article belongs to the Special Issue Developmental Programming of the Hypothalamus and Metabolic Systems)
►▼ Show Figures

Graphical abstract

12 pages, 932 KiB  
Article
Increased Fibroblast Growth Factor 21 (FGF21) Concentration in Early Second Trimester Amniotic Fluid and Its Association with Fetal Growth
by Nikolaos Vrachnis, Savvas Argyridis, Dionysios Vrachnis, Nikolaos Antonakopoulos, Georgios Valsamakis, Christos Iavazzo, Dimitrios Zygouris, Nikolaos Salakos, Alexandros Rodolakis, Nikolaos Vlahos, George Mastorakos, Peter Drakakis and Zoi Iliodromiti
Metabolites 2021, 11(9), 581; https://doi.org/10.3390/metabo11090581 - 28 Aug 2021
Cited by 4 | Viewed by 2278
Abstract
Altered fetal growth, either reduced or exacerbated, is associated with adverse perinatal outcomes. The underlying pathogenetic mechanisms of altered growth remain unclear. Fibroblast growth factor 21 (FGF21) and insulin are both considered to be major regulators of tissue growth and metabolism. The aim [...] Read more.
Altered fetal growth, either reduced or exacerbated, is associated with adverse perinatal outcomes. The underlying pathogenetic mechanisms of altered growth remain unclear. Fibroblast growth factor 21 (FGF21) and insulin are both considered to be major regulators of tissue growth and metabolism. The aim of our study was to investigate the association of second trimester amniotic fluid FGF21 and insulin concentrations with fetal growth. The amniotic fluid concentrations of FGF21 and insulin were determined in 80 cases of different fetal growth patterns (SGA—small for gestational age, LGA—large for gestational age, and AGA—appropriate for gestational age fetuses). Both peptides were found to be increased in cases of abnormal fetal growth, reduced growth velocity (SGA), or macrosomia (LGA). Specifically, FGF21 was significantly increased, as higher FGF21 levels were observed in the amniotic fluid of SGA and LGA fetuses compared with AGA fetuses (p < 0.05). Furthermore, the more severe the fetal smallness, the higher the FGF21 levels (p < 0.05). Similarly, higher insulin levels were noted in the amniotic fluid of SGA and LGA fetuses compared with those in AGA fetuses, though this was not statistically significant (p > 0.05). Again, the more severe the reduced fetal growth, the higher the insulin levels. Full article
(This article belongs to the Special Issue Developmental Programming of the Hypothalamus and Metabolic Systems)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop